Kelley Sheila P, Moynihan Jan A, Stevens Suzanne Y, Grota Lee J, Felten David L
Center for Psychoneuroimmunology Research, University of Rochester Medical Center, 300 Crittenden Boulevard, 14642, Rochester, NY, USA.
Brain Behav Immun. 2003 Apr;17(2):94-109. doi: 10.1016/s0889-1591(02)00101-0.
In susceptible strains of mice, the LP-BM5 mixture of murine retroviruses induces the fatal immunodeficiency disease known as murine acquired immunodeficiency syndrome (murine AIDS or MAIDS). We have previously reported that murine AIDS produces a profound depletion of splenic norepinephrine (NE). Here, we demonstrate that NE depletion is limited to the spleen, a major site affected by LP-BM5 infection. NE depletion in the spleen is first observed at two weeks following LP-BM5 inoculation, concurrent with the onset of splenomegaly, and continues through 12 weeks post-infection. Neuroanatomical studies revealed that the reduction in NE is due to destruction of splenic sympathetic nerve fibers. Administration of the NE reuptake blocker desipramine did not prevent LP-BM5-induced NE depletion, suggesting that destruction is not caused by excess release and reuptake of NE. Elucidating the mechanism of MAIDS-induced sympathetic nerve destruction may provide insight into autonomic and peripheral neuropathies reported in people with AIDS.
在易感染的小鼠品系中，鼠逆转录病毒的LP - BM5混合物会引发一种致命的免疫缺陷疾病，即鼠获得性免疫缺陷综合征（鼠艾滋病或MAIDS）。我们之前曾报道，鼠艾滋病会导致脾脏去甲肾上腺素（NE）大量减少。在此，我们证明NE的减少仅限于脾脏，这是受LP - BM5感染影响的主要部位。脾脏中的NE减少在LP - BM5接种后两周首次观察到，与脾肿大的开始同时出现，并持续到感染后12周。神经解剖学研究表明，NE的减少是由于脾交感神经纤维的破坏。给予NE再摄取阻滞剂地昔帕明并不能预防LP - BM5诱导的NE减少，这表明破坏不是由NE的过度释放和再摄取引起的。阐明MAIDS诱导的交感神经破坏机制可能有助于深入了解艾滋病患者中报道的自主神经和周围神经病变。
